V. Review of Alan R.Yurko’s Jury Trial, & Analysis of the Expert
Witnesses’ Testimonies and the State’s Claim
Alan R. Yurko’s jury trial took place February 22 to 24, 1999 in
the state of Florida . The prosecutor provided four major witnesses
testifying for the state, and (following the defense witness) two of these
were called for repeat appearances before the jury. Against these four,
the defense provided a single witness. The state witnesses were: 1) Dr.
Shashi B. Gore, the medical Examiner; 2) Dr. Gary Pearl, a consultant
neuropathologist (testified twice); 3) Dr. Ben Guedes, the treating physician;
and 4) Dr. Matthew A. Seibel, a general pediatrician (testified twice).
The defense witness was Dr. Douglas Radford Shanklin, a pathologist. In
addition, two radiologists, Dr. James Edward Hannah and Dr. Robert Scott
Mahan, testified in relation to the fractured rib #6; and Dr. Robert Gold,
ophthalmologist, gave testimony in relation to the minor bleeding in the
state witnesses (Gore, Guedes, and Seibel) stated that baby Alan died
as the result of Shaken Baby Syndrome. However, none of them provided
medical evidence to prove their case, and their testimonies were based
only on a theory. Dr. Pearl stated that the injuries in the brain and
spinal cord were acute injuries and did not start at birth or after birth.
He did not say that these injuries were caused by Shaken Baby Syndrome.
His findings are discussed in Section V-C, below.
In the previous section (IV) of this report is a review and analysis of
the medical examiner autopsy report and his testimony in court relating
to this case. They clearly show that Gore did not review all the medical
evidence, and he did not prove his case. In addition, he described the
histology of the heart, even though the heart had been donated for transplantation
prior to his examination. Also, in court he stated that the cerebrospinal
fluid was mixed with blood, but in his report he stated that the CSF was
clear. In this section, I present my review and analysis of the testimonies
of the other three state witnesses. This presentation shows that these
witnesses also did not review all the evidence and did not provide the
medical evidence to prove their case. I also present my review of the
defense witness. He made important contributions to this case.
Review of Dr. Ben Guedes’ testimony
Dr. Ben Guedes stated in court that baby Alan died as a result of “Shaken
Baby Syndrome.” His theory was that shaking the head caused bleeding,
and that the blood pushed on the brain causing an increase in pressure.
The pressure on the brain stem caused unconsciousness and cessation of
breathing. Dr. Guedes presented his conclusion about the cause of death
without making any attempt to review Francine’s medical record during
her pregnancy with Alan, the baby’s medical records from birth until
his hospitalization on November 24, 1997, the adverse reactions to vaccines
and medications given to the baby, and the autopsy findings. I explained
these issues and their impact on Alan’s health in sections I through
IV of this report. It is very clear that Guedes’ conclusion about
the cause of death was based on a theory and not on facts, because he
did not evaluate the medical evidence related to this case.
Furthermore, Guedes presented in court only selected items of his clinical
findings related to baby Alan’s five days in the Princeton and Florida
hospitals. He did not reveal that, at the time of his admission to Princeton
Hospital, Alan had diabetes and complications of diabetes, such as gastric
ulcer, metabolic acidosis, elevated anion gap, dehydration, anemia, elevated
serum liver enzymes and LDH (Table
12). Furthermore, Guedes did not reveal to the court that he treated
baby Alan with a long list of medications that included three types of
antibiotics, Tylenol, Motrin, heparin, antidiuretic hormones, potassium,
and others (Table
11). The clinical findings during Alan’s hospitalization
on November 24th through 29th, along with an analysis of the clinical
events are presented in Section III of this report. Below is a brief summary
of these clinical findings to show that Guedes was aware that baby Alan
had diabetes, hypokalemia, metabolic acidosis, infections, and dehydration,
because he reviewed the data and treated him for these conditions. Unfortunately,
his treatment with excessive doses of sodium bicarbonate and heparin caused
severe hypoxia and severe bleeding in the brain, lungs, and spinal cord.
Dr. Guedes examined baby Alan at Princeton Hospital shortly after his
admission. He saw the baby at about 12:30 PM on November 24, 1997 in the
emergency room after the emergency department physicians resuscitated
him. The baby arrived at Princeton with cardiac arrest and apnea. Dr.
Guedes’ initial evaluation revealed that baby Alan was flaccid, his
abdomen was soft and somewhat distended, and there was no bowel sound.
The baby developed bleeding from the gastrostomy tube due to a gastric
ulcer. His corneas were somewhat cloudy. Guedes also reviewed the result
of the first laboratory work done at Princeton. The first blood gas was
done at 12:09 PM showing a pH of 7.179, a PCO2 of 74 mm Hg, and a PO2
of 585 mm Hg (Table
Other laboratory work drawn at 12:09 PM showed a glucose of 337 mg/dL,
LDH of 2411 IU/L, SGOT of 207 IU/L, SGPT of 121 IU/L, a CO2 of 13 mEq/L,
anion gap of 22 mEq/L, and potassium of 4.9 mEq/L. The white blood cell
count was 20,900 per µL, hematocrit 25.3%, hemoglobin concentration
7.8 g/dL, and the platelet count was 571,000 per µL (Table
tests clearly showed that the baby suffered from diabetes, metabolic and
respiratory acidosis, bacterial infections, anemia, and liver and heart
damage. In Princeton Hospital, Dr. Guedes treated the baby with sodium
bicarbonate to control acidosis; three types of antibiotics—rocephin,
gentamicin, and Claforan (cefotaxime sodium)—to control bacterial
infection; and saline to treat dehydration (Table 6). He also treated
Alan in Florida Hospital on November 24 through November 28, 1997. He
gave the baby antibiotics, Tylenol, Motrin, sodium bicarbonate, potassium
chloride, heparin, dopamine, adenosine, muscle relaxant, antidiuretic
hormone, and other medications (Table
11). The baby responded very well to antibiotics. His temperature,
white blood cell count, and blood glucose levels returned to normal following
two days of treatment (Tables 8, 12, Table
On November 26th, his serum glucose level dropped to a normal level of
95 mg/dL from the level of 397 mg/dL (76% reduction) on November 24, 1997.
Also, on November 26th, the LDH, alkaline phosphate, and SGPT levels dropped
by 70%, 47%, and 19% respectively from their levels on November 24. On
11/26, the total white blood cell count was reduced by 35% from its level
on November 24th. This clearly indicates that the baby had liver and pancreas
bacterial infections, and that his infections were resolved because of
the treatment with antibiotics (Table
Unfortunately, Dr. Guedes treated Alan with heparin at 2:45 PM on November
24th, at a dose level of 2 cc (50% concentration of 1000 IU/ml) per hour
by intravenous infusion. The baby’s weight was 4.57 kg and the estimated
heparin dose was 219 IU/kg per hour. Based on this dose, the estimated
total dose of heparin infused up to the time of the CT scan (five hours)
was 1095 IU/kg, which is about 8.8 times the recommended maintenance dose
for infants of 125 IU/kg per five hours, recommended by the Physicians’
Desk Reference . Hemorrhage can occur virtually at any site in patients
receiving heparin. Patients suffering from anemia, any unexplained symptoms,
and/or having low blood pressure are at the greatest risk of having serious
hemorrhagic events following a therapeutic dose of heparin. Alan had hypotension,
and his hematocrit was very low (25.3%). In addition, the baby was treated
with adenosine, which is a potent vasodilator in most vascular beds, causing
significant hypotension (Table
11). Heparin also induces the formation of white clot due to the
aggregation of platelets. At 3:15 PM, at about 30 minutes post heparin
infusion, blood analysis showed increased prothrombin time and fibrinogen
split product (Table
9). The treatment with heparin explains the bleeding seen on the
CT scan taken at 7:50 PM on November 24th and the fall in the platelet
count seen on November 25th (Table
Furthermore, the bleeding in the brain was made worse by Alan’s second
treatment with heparin at 8:00 AM on November 25th. The baby was given
heparin by infusion similar to the dose given the day before (described
above, 219 IU/kg per hour). This treatment was not justified at all, because
heparin at a high therapeutic dose should not be given to any patient
suffering from bleeding and hypotension . Baby Alan had a bleeding
gastric ulcer, subdural hemorrhage, bleeding in the brain, and hypotension.
The platelet count prior to the administration of heparin on November
24th was 571,000/µL of blood and dropped to 397,000/µL (30%
reduction) at 5:45 AM on November 25, 1997 (at about 15 hours following
the start of the first heparin infusion). Heparin increases the tendency
of the platelets to aggregate and form a clot. Blood analysis values for
November 24th through November 27th are presented in Table
12. Alan also suffered from disseminated intravascular coagulation
(DIC) as a result of his treatment with heparin. At 3:15 PM, at about
30 minutes post heparin infusion, blood analysis showed increases in fibrinogen
split product (160 µg/mL) and prothrombin time (11.6 seconds). These
values are 1600 % and 115% of normal respectively, and they returned to
normal on November 26th following the cessation of the treatment with
make matters even worse, Dr. Guedes treated the baby with excessive amount
of sodium bicarbonate by IV to treat acidosis. This treatment caused severe
metabolic alkalosis, and the blood pH reached a very critical high level
of 7.7. This treatment caused severe hypoxia by preventing the hemoglobin
from releasing oxygen to the tissues; it caused reduced potassium level
in the blood, and caused cerebral edema, as explained in sections III
and IV of this report. Alan’s blood pH was 7.1 and serum potassium
level was 4.9 mEq/L on November 24th. The potassium dropped to critical
low of 2.3 mEq/L at 5:45 AM on 11/25 following the treatment with excessive
amount of sodium bicarbonate. The blood pH was at critically high levels
Dehydration, polyurea, weight loss, and wasting are symptoms and complications
of diabetes mellitus. In the first twenty-four hours, baby Alan’s
input was 725.8 mL, while his output during this period was 786 mL. Net
output was 60.2 mL. On November 24th, Alan weighed 10.05 pounds, and on
November 29th, 9.0 lb. He lost 1.05 lb (10% of his weight) in five days
during his hospital stay despite treatment with relatively high volume
of fluid IV. Furthermore, his average serum creatinine on November 24th
was 0.45 mg/dL (75% of low normal value) and dropped to 0.2 mg/dL (33%
of low normal) on November 27th (Table
12). Low creatinine is an indicator of low muscle mass and wasting
In addition, the baby was treated with an antidiuretic hormone (DDAVP)
on November 28th to prevent dehydration (Table
13). DDAVP is a synthetic analog of the natural pituitary hormone
8-arginine vasopressin (ADH), an antidiuretic hormone affecting renal
conservation. This fact shows that he was responding to medication in
spite of being declared brain dead on November 27, 1997. Also, he was
able to maintain his body temperature at about normal levels following
his treatment with antibiotics. The treatment with antibiotics reduced
the blood white blood cell count from 20, 900 to 13, 600/µL and
body temperature from 105.8 F to 99.8 F. This indicates that his fever
was caused by bacterial infections and not by brain injury, as Guedes
Dr. Guedes and Florida Hospital contacted the Orange County Sheriff’s
Office and the Child Protective Office on November 24, 1997 and filed
a report of child abuse based on the assumption that baby Alan was injured
as a result of abuse by his father. Alan R. Yurko was arrested by officers
from the Orange County Sheriff’s Office on November 26, 1997, while
his son Alan was still alive in Florida Hospital. I found that the actions
of Dr. Guedes and Florida Hospital are not supported by any medical facts.
Their actions are tragic for Alan’s family and dangerous for the
Dr. Guedes assumed that Mr. Yurko was guilty of child abuse, yet his own
examination of baby Alan revealed no injuries caused by trauma. Also,
he did not wait to the end to see the result of the autopsy. In addition,
he did not review the adverse reactions of medications that he gave to
the baby on November 24th to see if the heparin and other medications
had something to do with bleeding in the brain. Then he gave more heparin
and sodium bicarbonate the next morning, which caused more bleeding. On
November 24th, the subdural bleeding was on the right side of the brain
only, and on November 29th, the bleeding was on the right and left sides
of the brain. Guedes gave excessive amount of heparin and sodium bicarbonate,
which can cause bleeding in any child who has hypotension, anemia, and
tissue inflammation similar to baby Alan’s. The medical practice
and action of Dr. Guedes make no ill child safe from bleeding in the brain
and other tissues. Also, no parent can be safe from being accused of killing
his or her child by shaking. His work should be investigated to stop these
horrible tragedies from happening to people!
Review of Dr. Matthew A. Seibel’s testimony
Dr. Matthew Seibel is a general pediatrician and consultant with the child
protection team based in the children’s hospital in Orlando. He examined
baby Alan and reviewed his chart on November 25th for about 30 to 45 minutes
in Florida Hospital, and declared that the baby was injured as a result
of child abuse. He gave his conclusion about the cause of injuries without
review of Francine’s medical records while pregnant with Alan, the
baby’s medical records from birth until his hospitalization on November
24, 1997, the adverse reactions to the vaccines and medications given
to baby Alan, or the autopsy findings. These issues and their impact on
this case are explained in sections I through IV of this report. Below
are the questions presented to Dr. Seibel in court by the State of Florida
and defense attorneys, and his answers to these questions . They clearly
show that he presented his conclusion based on a theory only and not based
on the medical evidence.
Examination and diagnosis:
The state: Where did you first examine the child?
Seibel: The one and only one time I examined him was in pediatric
intensive care unit at Florida South on November 1997.
The state: And once you examined him and reviewed his medical chart,
did you have a diagnosis?
The state: What was that?
Seibel: The child had received inflicted trauma that was seen as
both brain injuries as well as injuries to several ribs that is characteristic
of an abusive situation.
The state: As part of your examination of this child, would you
rule out any natural disease and causes in making your diagnosis?
Seibel: You always like to try to put a nice face on it and you
look as hard as you can to make sense of it, but I was not able to find
any natural diseases other than trauma to cause these injuries in this
Defense attorney: You talk about a few minutes, examining the child,
a few minutes looking at the x-rays, a few minutes reading the report.
Totally, how much time you spend examining this case?
Seibel: Probably there or at the hospital between a half hour and
Defense attorney: Did you make any attempts to get this child’s
prior medical records, prenatal record, anything like that.
Seibel: No sir, I did not .
Defense attorney: Did you look up the medical Examiner’s report?
Seibel: I have been made aware of it. I do not have it with me.
I do not remember reviewing it very, very carefully.
2. Diffuse axonal injury:
Defense attorney: In your report you talk about diffuse axonal
injury; is that correct?
Seibel: Yes, Sir, that is the current theories regarding these
children when there is significant bleeding in the brain as we saw in
Defense attorney: We are not talking about theories. In your examination
of this child you actually did not see diffuse axonal injury?
Seibel: No Sir, I did not.
3. Retinal hemorrhage:
Defense attorney: Do you know how much hemorrhage was found in
the child’s retina in this case?
Seibel: No, I do not.
Defense attorney: Do you know whether or not there was retinal
hemorrhage in both eyes or one eye?
Seibel: I am not sure which one or who did it.
4. Rib fracture:
The state: Are there fractures that can be the result of birth
The state: And what type of fractures would that be?
Seibel: The most common fractures that we see is fractures of the
clavicle which is the collar bone right here.
The state: Within a reasonable degree of medical certainty, rib
fractures are considered to be abuse?
Seibel’s answers to the questions in court said it all. He spent
only 30 to 45 minutes on the entire case. He did not see axonal injury.
He did not know about the bleeding in the retina. He did not evaluate
the child’s and mother’s medical records. He gave his conclusion
about the cause of injury on November 25th when the baby was still alive.
He said that the child had several rib fractures, but the medical records
showed the baby had only rib #6 fracture. Furthermore, my review of the
medical literature revealed that multiple rib fractures do occur during
labor. I presented the findings of four studies that show the occurrence
of ribs fracture during labor in Section IV-J of this report. Also, I
presented a study that showed fracture of long bones during labor. Seibel
stated that the child’s injuries were caused by trauma, but the examination
by Dr. Guedes on November 24th revealed no injuries due to trauma on the
head or the body of the baby, except for a minor bruise under the right
It is very hard to imagine that Dr. Seibel testified in a court on this
very serious matter based solely on a theory; without evaluating the medical
evidence and the related published medical literature. His testimony put
an innocent father in prison for life and destroyed the family’s
structure. I believe that his unscientific and unjustifiable actions resulted
in a tragedy which puts our society in danger. His actions should be investigated.
As previously explained in this report (sections III, IV), the bleeding
in the brain and other tissues in baby Alan resulted from his treatment
with excessive amounts of heparin and sodium bicarbonate in the hospital.
I reached my conclusions after spending more than two hundred and fifty
hours evaluating the medical evidence and the related published medical
information. Baby Alan’s case and similar cases are very complicated
medical matters, as shown by the information presented in this report.
They should be evaluated by using differential diagnosis prior to giving
any conclusion. I am certain that spending only 30 or 45 minutes on this
case, as Dr. Seibel did, could not lead to a valid conclusion. Physicians
should take all facts in to consideration when they are faced with a complicated
task such as this one.
Review of Dr. Gary Steven Pearl’s testimony
Dr. Pearl is a consultant neuropathologist working with the Medical Examiner’s
office. He examined the brain, spinal cord, and the eyes of baby Alan
grossly on December 19, 1997, and also prepared slides. His pathology
findings on the brain, spinal cord, and the right eye do not support the
medical examiner and other physicians’ claims that the bleeding in
the brain occurred in minutes or in a few seconds. Dr. Pearl examined
the hematoma in the subdural space of the brain and spinal cord and observed
the proliferation of fibroblasts in layers, clotted blood with no fibrosis,
and fresh blood. He estimated the age of the oldest portion of the subdural
hematoma to be two to five days . This means that the blood was released
in at least three stages, as described in Section IV-D of this report,
and this contradicts the theory of the other state witnesses that the
bleeding in the brain occurred in minutes or in a few seconds.
Pearl also stated that baby Alan suffered from disseminated intravascular
coagulation (DIC), which led to the hemorrhage in the subdural space,
and that the DIC was induced by brain injury. I agree with Dr. Pearl that
the baby suffered from DIC, as shown clinically (Table
12); but the reason for the DIC was the treatment with excessive
doses of heparin, as explained in this report (Sections III, IV). Dr.
Pearl missed the role of heparin in the bleeding in the brain and spinal
cord and in the formation of DIC because he did not review the baby’s
records and treatment chart during his five days in the hospital.
Furthermore, Dr. Pearl observed swollen blood vessels and acute degeneration
of nerve cells in the brain and spinal cord and stated that these are
signs of acute injuries. They occurred as a response to a brain injury.
I agree with Dr. Pearl that these lesions are signs of acute injuries
occurring within 2-5 days prior to autopsy, but these lesions were induced
by severe hypoxia caused by excessive treatment with sodium bicarbonate
on November 24th and 25th, by severe anemia, apnea, cardiac arrest, and
hypotension, as explain in this report (Sections III, IV). The treatment
with bicarbonate caused severe metabolic alkalosis. The blood pH was 7.7.
This prevents the hemoglobin from releasing oxygen to the tissues, and
it caused hypoxia and cerebral edema in this case. Brain edema was confirmed
at autopsy. Dr. Pearl missed the influence of these factors on the formation
of the lesions in the brain and the spinal cord because he did not review
Alan’s medical records.
Dr. Pearl also observed meningeal inflammation and called it hemogenic
meningitis (inflammation of the meninges resulting from the presence of
blood). He based his conclusion on the quantity and type of inflammatory
cells present in the inflamed tissue. This lesion lacked the presence
of neutrophils. I believe that Dr. Pearl’s interpretation of the
tissue changes is incomplete because he did not review the baby’s
medical records. The baby was treated with high therapeutic doses of three
types of antibiotics, and this treatment reduced the severity of the acute
inflammation observed at the time of autopsy. The swollen blood vessels,
the presence of edema in the brain, fever (105.8 F) and the elevated white
blood cell count (20, 900/µL) observed on November 24th (Table
12) indicate that the baby suffered from acute meningitis. However,
the severity of the acute inflammation in the tissue was reduced by the
treatment with high therapeutic doses of gentamicin, rocephin, and Claforan
(cefotaxime sodium) on November 24th (Table
The treatment with antibiotics reduced the blood white blood cell counts
from 20, 900 to 13, 600/µL and body temperature from 105.8 F to
Also, Dr. Pearl did not present evidence in court that showed diffuse
axonal injury. In addition, Dr. Gore's autopsy report makes no mention
of Dr. Pearl’s pathology findings on the brain, spinal cord, and
eyes. Other state witnesses also did not present any evidence in court
that showed diffuse axonal injury. However, they claimed that diffuse
axonal injury is characteristic of “Shaken Baby Syndrome” (SBS).
Hemorrhage in the retina is another claimed characteristic marker for
SBS. Dr. Pearl stated that the bleeding in the right retina was very minor
and did not impact his opinion in this case. Below are the defense attorney’s
questions presented to Dr. Pearl in court regarding the axonal injury
and the retinal bleeding, and his answers to these questions.
Diffuse axonal injury:
Defense attorney: Now, I believe you testified that there was some
slides that shows the diffuse axonal injuries?
Pearl: That is correct.
Defense attorney: Do you have those slides?
Pearl: I do not have any of the slides.
Defense attorney: But there were slides that was done that have
shown the diffuse axonal injury?
Pearl: There is a glass slide that does. I did not photograph that.
2. Bleeding in the retina of the right eye:
Defense attorney: Was there hemorrhage in the retina or behind
Pearl: There was a small hemorrhage.
Defense attorney: Minute?
Defense attorney: Was that significant?
Pearl: That wasn’t significant to me. Really did not impact
on my evaluation of the case.
Dr. Pearl did not review Francine’s medical records during her pregnancy
with Alan, the baby’s medical records from birth until his hospitalization
on November 24, 1997, or the adverse reactions of vaccines and medications
given to baby Alan. This limited his ability to interpret his pathology
findings and to provide valid conclusions about the causes of injury and
Review of Dr. Douglas R. Shanklin’s testimony
Dr. Shanklin, the defense witness evaluated the H & E stained tissue
sections of the brain and other organs and stated that baby Alan died
from natural causes. I agree with Dr. Shanklin that baby Alan suffered
from health problems at birth and following birth. These included respiratory
distress syndrome, jaundice, and growth retardation. However, these problems
did not cause his cardiac arrest or the bleeding in the brain and other
tissues observed in the autopsy. Alan’s cardiac arrest was caused
by hypokalemia developed as a result of metabolic and respiratory acidosis
due to diabetes and pneumonia. Alan’s health problems at birth and
following birth increased his susceptibility to develop adverse reactions
to vaccines. The six vaccines that he received on November 11, 1997 caused
his infections and diabetes, as explained in sections II and IV of this
report. The bleeding in the brain and other tissues was caused by the
excessive treatment with heparin and sodium bicarbonate given in the hospital,
as explained previously.
Shanklin made very important contributions to this case. He stated that
baby Alan’s kidneys were not fully developed. This finding may explain
the mother’s problem with oligohydramnios, as explained in section
II of this report. He also stated that the baby suffered from pneumonia
and meningitis in the brain region and the spinal cord. His findings may
explain the susceptibility of these regions to bleeding caused by the
treatment with heparin and sodium bicarbonate. The inflammation in these
regions affected the integrity of the blood vessels and caused predisposition
to the leakage of fluid and blood induced by treatment with excessive
doses of heparin and sodium bicarbonate. In addition, he described old
neurological injuries in the brain and spinal cord. I believe that the
high levels of bilirubin observed in the first week following birth caused
these injuries (Table
I addressed this issue in section II.
Analysis of the state’s claim
During Alan R. Yurko’s jury trial, the prosecutor, Ms. Wilkinson,
presented only one theory—that Baby Alan died as a result of “Shaken
Baby Syndrome” (SBS), and Mr. Yurko, the father of the child, did
it. My review of the medical evidence and the trial transcript revealed
that the prosecutor did not prove her case that the injuries were caused
by trauma and that Mr. Yurko abused his child. However, the prosecutor
achieved her goal of convicting Mr. Yurko of a horrible crime he did not
commit. He received a life sentence + 10 years. I believe that the prosecutor
used unfair practices and violated Mr. Yurko’s right of getting a
fair trial. Below is a list of the prosecutor’s unfair tactics and
evidence that shows the state did not prove its case.
The prosecutor presented trauma as the only possibility for the cause
of injuries in this case; but Dr. Guedes examined the baby on November
24th, and his examination did not reveal any injury caused by trauma,
except for the minor bruise under the right eyelid. In addition, Mr. Yurko
never stated that he abused his child, and no one observed him hurting
2. The prosecutor did not discuss the adverse reactions of vaccines
given to baby Alan (Table
5). The studies presented in section II of this report clearly
show that these vaccines caused severe adverse reactions, such as apnea,
cardiac problem, and respiratory infections, in premature infants. Baby
Alan developed diabetes resulting from an infection and complications
of his vaccination. This led to his cardiac arrest on November 24, 1997.
3. The prosecutor did not discuss the adverse reactions of medications
given to Alan on November 24th through November 29th. It is very obvious
that heparin causes bleeding at the doses given.
4. The prosecutor stated that the baby developed subdural bleeding
in the brain, retinal bleeding, and diffuse axonal injury as a result
of SBS. However, the autopsy and the pathology findings clearly show that
the subdural bleeding did not occur in a few minutes as the SBS theory
claimed. In addition, none of the state witnesses presented evidence in
court that they found diffused axonal injury. Also, the bleeding in the
retina of the right eye was very minor. Even Dr. Pearl stated that this
injury was very minute and had no impact on his evaluation.
5. The prosecutor did not ask Dr. Gore to provide the x-ray findings
to prove that Alan had fractures in ribs 5, 7, and 10. He stated in his
autopsy report that he used an x-ray to confirm his findings. In addition,
the prosecutor held the x-ray findings taken on September 16, 17, and
18 as proof that the rib fractures did not happen during labor. It takes
at least 7 days for the calluses to form, and on September 18, 1997, the
baby was 3 days old. However, the prosecutor did not accept the x-ray
findings of November 24th and 25th that the baby had only rib # 6 fracture.
She stated that the fractures are better seen at autopsy, but she overlooked
the fact that Dr. Gore stated in his report that he took the x-ray to
confirm the rib fractures. It seems that the prosecutor was trying to
select certain evidence to support her theory that the father was abusing
his son and caused multiple rib fractures. Her actions showed that she
did not conduct her business in a fair and impartial manner.
6. The prosecutor allowed Dr. Gore to present in court as evidence
of trauma two photographs of minor contusions in the temporal areas of
the head that occurred in the hospital about one day prior to autopsy.
The medical examiner’s main objective should be discussing the causes
of injuries that caused death in this case. I believe he used these photos
to influence the jury’s thinking that physical force was used, and
the prosecutor should not have allowed this.
7. None of the state witnesses evaluated all of the evidence relevant
to this case, such as prenatal records and the baby’s medical records
from birth until the time of his
cardiac arrest, and the prosecutor did not question the validity of their
VI. Conclusions and Recommendations
Alan Ream Yurko suffered from several serious heath problems at birth
and following birth, such as respiratory distress syndrome, hypoglycemia,
jaundice, growth retardation, and bacterial infections. His serum bilirubin
level was 17.4 mg/dL at 3 days post-birth, which is capable of causing
encephalopathy. Also, his risk of developing encephalopathy and of suffering
from hypoxia was increased by the treatment with antibiotics that bind
with albumin and release bilirubin. In addition, baby Alan had high risk
of developing congenital deformity of organs and the skeleton because
his mother suffered from gestational diabetes and oligohydramnios during
the pregnancy. His growth rate in the first month of life was poor, but
he showed a good improvement in his growth rate during the second month.
his pediatrician gave him six vaccines at two months of age and sent him
home without monitoring or medical supervision. It has been reported that
premature children, such as baby Alan, who were vaccinated prior to 70
days of age showed very high risk of developing serious health problems,
such as apnea, bradycardia, and oxygen desaturation, that required medical
intervention. Alan developed fever, reduction in food intake, lethargy,
and became irritable a few days following vaccination. The medical evidence
indicates that his vaccination induced these symptoms.
At thirteen days post vaccination, the baby had cardiac arrest and apnea.
The clinical tests revealed that he was suffering from diabetes mellitus
and the complications of diabetes, such as bacterial infections, gastric
ulcer, metabolic acidosis, hypokalemia, dehydration, anemia, weight loss,
loss of muscle tone, and cardiac arrest. The six vaccines received on
November 11, 1997 were the likely cause of his infections and diabetes
5). His cardiac arrest and apnea on November 24th, resulted from
hypokalemia which was a result of metabolic and respiratory acidosis.
It appears that his diabetes was induced by bacterial infections, because
his blood sugar level of 397 mg/dL on November 24th returned to normal
two days following IV antibiotics. He also had pneumonia, meningitis,
eye infection, and liver and heart damage. His liver serum enzymes and
LDH levels were also reduced significantly following the treatment with
antibiotics, and this indicates that he had liver, and maybe heart, bacterial
Unfortunately, at Florida Hospital baby Alan was treated on November 24
and 25, 1997 with high doses of sodium bicarbonate that caused metabolic
alkalosis (pH 7.7) and severe hypoxia. He was also treated with high doses
of heparin that caused bleeding in tissues. Heparin caused severe subdural
bleeding in the brain and spinal cord, minor bleeding in the brain and
the retina of the right eye, and bleeding in the lungs. It also caused
disseminated intravascular coagulation (DIC). I am very surprised to see
that Dr. Guedes treated Alan with high doses of sodium bicarbonate and
heparin at 8:00 AM on November 25th despite the fact that he was suffering
from severe metabolic alkalosis (PH 7.61-7.7) and bleeding in the brain
and subdural space (Table
11). Treatments with high doses of sodium bicarbonate and heparin
were not medically justified.
The treatment with bicarbonate for individuals with diabetes should stop
at pH 7.2, and this treatment carries high risk of causing cerebral edema,
as happened in this case. Heparin should not be given to patients suffering
from bleeding, hypotension, and anemia, because of the high risk of bleeding
in such patients associated with heparin. Baby Alan had hypotension, anemia,
hypoxia, bacterial infections in several organs, bleeding gastric ulcer,
and bleeding in several organs. It seems that Dr. Guedes overlooked the
adverse reactions of sodium bicarbonate and heparin, as well as the recommendations
presented in the PDR and medical textbooks concerning the treatment with
The radiology findings of November 24 and 25, 1997 showed that Alan had
only rib #6 fracture. Rib fractures have been observed to occur during
labor even in mature babies. Also, oligohydramnios can cause positional
skeletal deformity. The medical evidence indicates that the fracture of
rib #6 most likely happened during labor. The claim of Dr. Gore that the
baby had additional ribs fractures is not valid, because he did not provide
any evidence to support his claim, such as x-ray results and films. In
addition, there were no calluses observed in the cut sections of the swollen
cartilage at autopsy.
Dr. Gore’s autopsy report and his court testimony related to this
case suffer from accuracy problems and contain very serious contradictions.
They are certainly not reliable medical evidence to be used to answer
questions about the cause(s) of death. He stated that the heart was normal
and described the histology of the heart, but in the same report, he mentioned
that the heart was donated prior to his examination. This indicates that
Gore was describing the heart of a different child and got his cases mixed
up. This is very serious, and his work should be investigated. Also, he
stated in his report that the cerebrospinal fluid was clear; whereas,
in court he said that the CSF fluid was mixed with blood. This is another
serious problem found in Gore’s work.
In addition, Gore said in court that the baby did not have meningitis,
but his report does not contain any description of the histology of the
meninges to show that he examined them. The other two pathologists who
evaluated the slides of the meninges observed acute changes that indicate
meningeal inflammation. Furthermore, he reported that the baby’s
head circumference was 22 cm, and that is obviously wrong. It was 37.5
cm eighteen days prior to the autopsy date.
Furthermore, Gore did not provide the medical evidence in his report and
in court to support his conclusion that baby Alan died as a result of
“Shaken Baby Syndrome.” Gore stated that the subdural bleeding
in the brain occurred in a few minutes or even in a few seconds due to
vigorous shaking. However, the autopsy and the pathology findings showed
that the bleeding occurred during 2-5 days and at least in three stages.
The bleeding also occurred in the spinal cord and the lungs, which has
nothing to do with the SBS theory, but it indicates that the bleeding
resulted from cardiovascular problems. In addition, he did not show any
evidence that the baby had diffuse axonal injury in the brain. No description
of axonal injury was presented in his report, and he did not show a single
slide describing such a lesion during the trial. The other three state
witnesses also did not show any slide or picture of an axonal injury.
Furthermore, I find Gore’s conclusion about the cause of death invalid,
because he did not review the baby’s prenatal records, the mother’s
records during her pregnancy with Alan, or adverse reactions of vaccines
and medications given to the baby. He missed the facts that the baby had
diabetes, hypokalemia, anemia, metabolic alkalosis, bleeding as a result
of heparin treatment, and hypoxia and cerebral edema due to the treatment
In addition, my review of the medical literature revealed that axonal
injury in the brain and spinal cord can occur in cases of cardiac arrest,
edema, hypoglycemia, and from other causes; and it is not necessarily
a characteristic lesion of injuries caused by trauma. Also, treatment
with high doses of heparin and sodium bicarbonate can induce bleeding
in cases of hypotension, anemia, and inflammation in tissues, as happened
in this case. Heparin and sodium bicarbonate are commonly-used agents
to treat clotting disorder and acidosis. Therefore, cases of SBS should
be investigated to rule out the contribution of therapeutic agents and
other factors in the pathogenesis of brain lesions. I believe that cases
of individuals who were convicted of killing babies by SBS based on the
axonal injury, subdural bleeding, and eye bleeding should be reexamined.
Also, I believe that Gore’s action of presenting in court two photographs
of minor contusions that occurred in the hospital, which were unrelated
to the cause of death, is scientifically and professionally unjustified.
I believe that he did it to influence the thinking of the jury that physical
force had been used on the baby.
My review of the evidence indicates that Dr. Guedes’ testimony in
court is unsupported by science and medical facts. He did not review the
medical evidence related to this case such as prenatal record, the baby
medical record, and the pathology findings. In addition, he did not review
related published literature describing the adverse reactions to vaccines
and medications given in this case. Also he did not reveal to the court
that the baby was treated with three types of antibiotics to fight infections,
bicarbonate and heparin; and that the baby suffered from diabetes, dehydration,
hypokalemia and complications of diabetes. I believe that withholding
of these vital data from the court resulted in a negative outcome of the
trial, and this issue should also be investigated.
Dr. Guedes’ treatment of baby Alan with high doses of bicarbonate
and heparin caused serious injuries and death and should be investigated.
In addition, this treatment produces bleeding in the brain and other tissues
and axonal injuries, which are considered by the proponent of SBS as characteristic
markers for it. It led to the false conviction and the imprisonment of
I believe that Dr. Seibel’s testimony in court was also unsupported
by medical evidence and science, based on the facts that he did not review
the medical evidence that related to this case such as prenatal record,
the baby medical record and the related published literature describing
the adverse reactions to vaccines and medications given, and the pathology
findings. He spent only 30-40 minutes on this case, and this certainly
did not give him the expertise to testify on this complicated medical
Alan Yurko and his family suffered two tragedies as a result of problems
with our current medical system regarding the vaccination of premature
babies, the treatment given to baby Alan in the hospital, and the approaches
of the state witnesses in evaluating the evidence in this case. The first
tragedy is the loss of baby Alan because of adverse reactions to vaccines
and the excessive doses of heparin and sodium bicarbonate given in the
hospital. It seems that his pediatrician was unfamiliar with the adverse
reactions of vaccines in premature children. He gave him six vaccines
and sent him home. Dr. Guedes also overlooked the adverse potentials of
heparin and bicarbonate. These issues should be addressed by the state
and medical authorities, which might save babies from death due to adverse
reactions to vaccines and treatment with the wrong medications.
The Yurkos’ second tragedy was the conviction of Mr. Yurko with a
horrible crime he did not commit. He was convicted because the state’s
four expert witnesses did not take the time to review the evidence and
the related published literature. Nor did they sort out the facts, so
that their testimonies were based on a theory only. The prosecutor contributed
to the problem by focusing on only one theory. She also allowed Gore to
present evidence that had no connection to the case such, as the photographs
describing the two contusions on the baby’s head.
I believe that the state of Florida has the responsibility to review the
evidence presented in this report. It shows that Mr. Yurko is innocent,
and they should take speedy action to free him from prison. Also, the
state should investigate the involvement of the state witnesses and the
prosecutor with similar cases resulting in the conviction of parents accused
of killing their children by SBS. Furthermore, I believe that the state
and the doctors who caused the Yurko’s tragedy should compensate
Mr. Yurko and his family for the loss of their child, their suffering,
and the expenses paid.
objective of the state and the medical system should be determining the
factual causes that led to the illness and death of a child and to prevent
such problems from happening to other children. Accusing innocent parents
of abusing and killing their children based on unsupported theory, as
it happened in this case, will not prevent the death of other children
by vaccines and incorrect medications. But it certainly puts innocent
people in prison and causes suffering. It also costs the taxpayers huge
sum of money to pay for trials and legal fees. I spent more than 250 hours
working on the Yurko case to find the factual causes of death and to write
the detailed report. I hope that the state of Florida, the medical system,
and our society will take advantage of this opportunity to see the real
problems facing a premature baby who received vaccines and was not properly
monitored by the medical community. This tragedy affects not only the
child, but also its family and the rest of the world.
Medical records of Francine Ream (1997). Florida Hospital, Orlando Florida.
 Medical records of Francine Ream (1997). Birthing Cottage of
Inc., 434 Grove Avenue, Winter Park, Florida.
 Medical records of Francine Ream (1997). Fairview Hospital,
 Buttram, HE, M.D. and Yazbak, E., M.D. Shaken Baby Syndrome
or Vaccine-Induced Encephalomyelitis? The Story of Baby Alan.
 Yurko, Alan R. Hyperbilirubinemia and Kernicterus in the
Case of Alan Yurko.
 Sanchez PJ, Laptook AR, Fisher L, Sumner J, Risser RC, Perlman
JM. Apnea after immunization of preterm infants. J Pediatr 1997;
 Harrison’s Principles of Internal Medicine. 14th
edition. Editors: Fauci AS, Braunwald E, Isselbacher KJ, Wilson JD, Martin
JB, Kasper DL, Hauser SL, Longo DL. McGraw-Hill, New York, 1998.
 Pathology, Second Edition. Editors: Rubin, E and Farber,
JL. J. B. Lippincott Company, Philadelphia, 1994.
 Williams Obstetrics, 21st Edition, 2001. Editors: Cunningham
FG, Gant NF, Leveno KJ, Gilstrap LC, Hauth JC, Wenstrom KD. McGraw-Hill,
 Neonatal-Perinatal Medicine, Volume 1, Seventh edition,
2002. Editors: Fanaroff AA and Martin RJ. Mosby, St. Louis, Missouri.
 Pathologic Basis of Disease, Third edition, 1984. Editors:
Robbins SL, Cortran RS, and Kumar V. W. B. Saunders Company, Philadelphia,
 Neonatal-Perinatal Medicine, Volume 2, Seventh Edition,
2002. Editors: Fanaroff AA and Martin RJ. Mosby, St. Louis, Missouri.
 Jury Trial Document for the trial of Alan Yurko, February
22-24, 1999. Orlando, Florida.
 Chauhan SP, Sanderson M, Hendrix NW, Magann EF, Devoe LD.
Perinatal outcome and amniotic fluid index in the antepartum and intrapartum
periods: A meta-analysis. Am J Obstet Gynecol 1999 Dec;181(6):1473-8
 Voxman EG, Tran S, Wing DA. Low amniotic fluid index as a
predictor of adverse perinatal outcome. J Perinatol 2002 Jun;22(4):282-5.
 Doctors charts for Alan Ream Yurko, weekly exams for October
10, 1997 through November 11, 1997.
 Physicians’ Desk Reference, Edition 53, 1999.
Medical Economics Company, Inc, Montavale, NJ, USA.
 Sen S, Cloete Y, Hassan K, Buss P. Adverse events following
vaccination in premature infants. Acta Paediatr 2001; 90(8):916-20.
 Botham SJ, Isaacs D, Henderson-Smart DJ. Incidence of apnoea
and bradycardia in preterm infants following DTPw and Hib immunization:
a prospective study. J Paediatr Child Health 1997; 33(5):418-21
 Slack MH, Schapira D. Severe apnoeas following immunisation
in premature infants. Arch Dis Child Fetal Neonatal Ed. 1999; 81(1):F67-8.
 Botham SJ, Isaacs D. Incidence of apnoea and bradycardia in
preterm infants following triple antigen immunization. J Paediatr Child
Health 1994; 30(6):533-5.
 Braun MM, Mootrey GT, Salive ME, Chen RT, Ellenberg SS. Infant
immunization with acellular pertussis vaccines in the United States: assessment
of the first two years' data from the Vaccine Adverse Event Reporting
System (VAERS). Pediatrics 2000; 106(4):E51  Medical records
of Alan Ream Yurko (1997). Princeton Hospital, Florida.
 Medical records of Alan Ream Yurko (1997). Florida Hospital,
 Spurgeon D. Study shows which children at greatest risk of
cerebral oedema in diabetic crisis. BMJ 2001; 322:258.
 Glaser N, Barnett P, McCaslin I, Nelson D, Trainor J, Louie
J, Kaufman F, Quayle K, Roaback M, Malley R, and Kuppermann N. Risk factors
for cerebral edema in children with diabetic ketoacidosis. N Engl J
Med 2001; 344:264-69.
 Bureau MA, Begin R, Berthiaume Y, Shapcott D, Khoury K, and
Gagnon N. Cerebral hypoxia from bicarbonate infusion in diabetic acidosis.
Journal of Pediatrics 1980; 96:968-73.
 Shashi B. Gore, MD, MPH, autopsy report for Alan Ream-Yurko
(sic), case # MEH-1064-97, 1997. Office of The Medical Examiner, District
Nine, 1401 Lucerne Terrace, Orlando, Florida 32806-2014.
 Dolinak D, Smith C, Graham DI. Hypoglycaemia is a cause of
axonal injury. Neuropathol Appl Neurobiol 2000; 26(5):448-53.
 Dolinak D, Smith C, Graham DI. Global hypoxia per se is an
unusual cause of axonal injury. Acta Neuropathol (Berl) 2000; 100(5):553-60.
 Kaur B, Rutty GN, Timperley WR. The possible role of hypoxia
in the formation of axonal bulbs. J Clin Pathol 1999; 52(3):203-9
 Oehmichen M, Meissner C, Schmidt V, Pedal I, Konig HG. Pontine
axonal injury after brain trauma and nontraumatic hypoxic-ischemic brain
damage. Int J Legal Med 1999; 112(4):261-7.
 Oehmichen M, Meissner C, Schmidt V, Pedal I, Konig HG, Saternus
KS. Axonal injury--a diagnostic tool in forensic neuropathology? A review.
Forensic Sci Int 1998; 95(1):67-83.
 Shannon P, Smith CR, Deck J, Ang LC, Ho M, Becker L. Axonal
injury and the neuropathology of Shaken Baby Syndrome. Acta Neuropathol
 Hartmann RW Jr. Radiological case of the month. Rib fractures
produced by birth trauma. Arch Pediatr Adolesc Med 1997; 151(9):947-8.
 Rizzolo PJ, Coleman PR. Neonatal rib fracture: birth trauma
or child abuse? J Fam Pract 1989; 29(5):561-3.
 Cumming WA. Neonatal skeletal fractures. Birth trauma or child
abuse? J Can Assoc Radiol 1979; 30 (1):30-3.